In a mouse TNBC model, loss of function of ubiquitin-specific peptidase 9x-linked (USP9x) in tumor cells abolished NICD activation reduced the production of proinflammatory cytokines (e.g., CCL2, IL-1β), which further reduced the tumor inflammation through inhibiting the infiltration of CD206+ TAMs and Treg cells, augmenting the anti-tumor immune response through increase the infiltration of CD8+ T cells, suppressing BC tumor cell growth in vivo [141]. The gene discussed is IL1B; the disease is neoplasm.